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Query: UMLS:C0012833 (dizziness)
 9,689 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Blood pressure, which ist the product of cardiac output and peripheral vascular resistance is regulated by a complex feedback mechanism involving the sympathetic and parasympathetic systems and hormones. An acute disturbance of regulation may lead to a life-threatening increase in blood pressure. Diagnosis is based upon a careful measurement of blood pressure, which must be performed under internationally standardized conditions. Hypertensive crisis refers to a rapid blood pressure increase greater than 30 mmHg above the age-related 95th percentile. The main causes of hypertension in childhood are renal diseases, which may be aggravated by additional conditions either by the clinician himself (e.g. cyclosporin, steroids) or by the patient (lack of compliance). Crisis affects the brain (hypertensive encephalopathy), the heart (left ventricular insufficiency), the retina (visual disturbances) and the mucous membranes (epistaxis). Hypertensive encephalopathy is induced by a break-through of the autoregulation of brain flow, leading to hyperperfusion and, thus to cerebral oedema. The clinical manifestations are characterized by restlessness, severe and diffuse headache, vomiting, nystagmus, impaired vision, dizziness, paraesthesia, seizures and palsies, which may lead - if untreated - to coma and death. The course is usually prolonged and reversible by adequate treatment. The morphological consequences are purpura cerebri, fresh retinal haemorrhages and papillary oedema, apart from left ventricular dilatation and hypertrophy. The diagnostic procedure rests on the quick realization of essential anamnestic (blood pressure, renal disease, drugs), clinical (oedema, cardiac action, central nervous system, fundus) and laboratory parameters (serum creatinine, electrolytes, glucose, blood count, urine). Treatment should start before the manifestation of clinical signs (hypertensive emergency) with rapidly acting antihypertensive drugs.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[The hypertensive crisis in childhood]. 305 87

A forty-year-old man was admitted to our hospital because of dizziness, palpitations and an oppressive feeling in the precordium. Physical examination was normal. A chest roentgenogram revealed mild cardiomegaly and the electrocardiogram showed ventricular tachycardia of a left bundle branch block configuration which was terminated by the intravenous injection of procainamide. During sinus rhythm the electrocardiogram showed incomplete right bundle branch block, PQ prolongation and inverted T waves in leads V1 through V3. Two-dimensional echocardiography revealed only moderate right ventricular dilatation. Right ventricular angiography showed severe right ventricular dilatation and hypokinesis of the right ventricular apex and pulmonary artery infundibulum. From these characteristics signs we concluded that this adult patient had arrhythmogenic right ventricular dysplasia (ARVD), suggesting that this condition is not confined to children but may occur in adults as well.
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PMID:An adult case of arrhythmogenic right ventricular dysplasia. 400 56

This study was undertaken to test the validity of methods of evaluating ventricular tachycardia and in therapeutic surveillance. One hundred and thirty nine patients aged 16 to 84 years, with and without severe ventricular arrhythmias (ventricular tachycardia, VT, and fibrillation, VF) were divided into two groups after clinical, echocardiographic and 24 hour Holter investigations: Group I comprised 26 patients with a least one documented attack of VT or VF; Group II comprised 113 patients without these arrhythmias, who complained of dizziness, syncope, and/or their ECG showed a conduction defect, and so electrophysiological investigation was undertaken. A protocol of ventricular stimulation was undertaken in addition to the usual measurements of conduction times, comprising incremental ventricular stimulation from 100 to 200/min, single and paired extrastimulus in sinus rhythm and during ventricular pacing at rates of 100 and 150/min, the first extrastimulus being programmed 10 ms after the end of the ventricular effective refractory period. Excluding bundle to bundle reentry, the following results were obtained: In Group I: VT was triggered 16 times (61,5 p. 100), and in 4 of these cases VF occurred and required defibrillation. Ten patients had previous myocardial infarction; 5 patients had left ventricular dilatation. In 2 cases runs of 3 or 4 VES were recorded. No arrhythmia could be induced in 8 cases (30,8 p. 100); 5 of these patients had apparently normal hearts. In Group II: VT (greater than 5 VES) was triggered in 22 cases (19,5 p. 100) and in 4 cases this degenerated to VF requiring defibrillation. 11 patients had apparently normal hearts; 6 patients had left ventricular dilatation and 4 patients had previous myocardial infarction. 1 to 4 repetitive VES were observed in 67 cases (59,3 p. 100): the heart was judged to be normal in all patients except those with previous infarction. No correlation was established between the ability to induce VT and age, syncope, or ECG changes (especially bundle branch block). However, a correlation was found between the induction of VT and underlying cardiac disease and the method of induction of VT; in Group II, all episodes of VT were triggered by delivering paired ventricular extrastimuli on a background paced rhythm. These results show that repetitive ventricular responses can easily be triggered and that this has no pathological significance.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Results of the systematic application of ventricular stimulation methods]. 642 12

We present a 81-year old male who developed dementia, gait disturbance and right hemiparesis. He was well until the age of 74 when he developed a hemorrhagic infarction in the right occipital region, which left him left homonymous hemianopsia. One year later he had one TIA attack consisting of dizziness, headache, and some clouding of consciousness. At that time, atrial fibrillation was found. At age 79, he was attacked by right hemiparesis. Cranial CT scans revealed a lesion consistent with a hemorrhagic infarct in the left middle cerebral artery territory. Two months prior to his final admission, he had a gradual onset of forgetfulness, labile affect, nocturnal agitation and hallucination which were followed by gait disturbance and urinary incontinence. On admission, he was alert but moderately demented. In addition he showed difficulty in repetition, limb kinetic and ideomotor apraxia of the left hand indicative of sympathetic apraxia, and constructional apraxia bilaterally. Granial nerves appeared intact except for left homonymous hemianopsia. His gait was wide-based and small stepped. No weakness or ataxia was noted. Deep reflexes were diminished on the left side. Plantar reflex was equivocally extensor of the left. Light touch and pain was slightly diminished on the right side. Cranial CT scans revealed a large low density area in the left fronto-temporo-parietal region. Also ventricular dilatation, diffuse low density change in the subcortical white matter, and diffuse cortical atrophy were seen. His clinical course was complicated by melena, anemia, pneumonia, cardiac failure and renal failure. He expired 2 months after his admission.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A 81-year-old man with dementia, gait disturbance, hemiparesis, and sympathetic apraxia]. 833 25

Fulminant myocarditis can lead to acute left ventricular dilatation and cardiogenic shock from heart failure. If hemodynamic stabilization cannot be achieved with maximized medical therapy, mechanical circulatory support becomes necessary. We here report on a 40-year-old patient who underwent emergent left ventricular assist device (LVAD) implantation (HVAD, HeartWare) in cardiogenic shock level 1 (Interagency Registry for Mechanically Assisted Circulatory Support). He quickly recovered and was fully active during follow-up. After 6 months, he first noticed palpitations and experienced episodes of dizziness, which were found to be caused by recurrent ventricular tachycardias. Echocardiography demonstrated a markedly remodeled and downsized left ventricle with improved function. A mechanical irritation of the HVAD inflow touching the inferior-posterior wall was found to trigger these focal arrhythmias. The HVAD was explanted, and no further arrhythmias occurred.
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PMID:Mechanically induced ventricular tachycardia by the HeartWare ventricular assist device. 2427 Feb 35